预适应和后适应在脑缺血治疗中的共同靶点

The common targets of preconditioning and postcondifioning in the treatment of cerebral ischemia

作为机体的一种内源性保护措施，预适应和后适应在缺血再灌注过程中可能发挥着共同的保护机制，如减少氧自由基生成、激活腺苷受体、内生性一氧化氮和热休克蛋白产生增多、抑制免疫炎性反应和神经元凋亡、激活细胞内信号转导通路、线粒体敏感钾通道开放以及线粒体渗透性转导孔的关闭。研究这些机制中的共同靶点，可为开发新药物和减少缺血再灌注损伤提供新的理论依据。

As an endogenous organism protective measure in vivo, preconditioning/ postconditioning in the process of ischemia/reperfusion may play common protective mechanisms, such as reducing the generation of oxygen free radicals, activating adenosine receptor, increasing endogenous nitric oxide and heat shock protein, inhibiting immune inflammatory response and neuronal apoptosis, activating intracellular signal transduction pathways, opening mitochondrial ATP-seusitive potassium channels, as well as closing mitochondrial permeability transition pores. Investigating the common target of these mechanisms may provide a new theoretical basis for developing new drugs and reducing ischemia/reperfusion injury.